Tumor Invasion And Metastasis Term Paper

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Tumor Invasion and Metastasis Tumor Invasion

This is a paper that concentrates on tumor invasion and metastasis. There are five references used for this paper.

Cancer is one of the deadliest diseases faced by mankind today. It is important to look at tumor invasion and metastasis to understand how cancer can spread and ways in which the progress of cancer can be arrested.

Tumor Invasion

A substantial problem in the treatment of carcinoma patients is tumor invasion and metastasis. Approximately "30% of patients with newly diagnosed solid tumors already have clinically detectable metastases (herkules.oulu.fi/isbn9514254023/html/x446.html)." The production of "extracellular matrix degrading enzymes, such as serine proteinases, metalloproteinases, cysteine proteinases, threonine proteinases, and aspartic proteinases (herkules.oulu.fi/isbn9514254023/html/x446.html)" is linked with tumor invasion.

The transition from "in situ tumor growth to mestastic disease is defined by the ability of tumor cells at the primary site to invade local tissue and to cross tissue barriers (http://www.harcourt-international.com/e-books/pdf/478.pdf)." The process begins when neoplastic cells infiltrate "the basement membrane and invade the interstitial stroma by active protolysis. Intravasation requires tumor cell invasion of the subendothelial basement membrane, in a similar manner as tumor cell extravasation occurs in the distant organ (http://www.harcourt-international.com/e-books/pdf/478.pdf)."

Metastasis

Metastasis is the "transfer of a disease from an organ of a body to another not related to it. The spread of cancer cells to distant sites implies a complex series of cellular abnormalities caused, in part, by genetic aberrations (Van Noorden, 1998 )."

The majority of cells in the body are held "tightly in place by molecular tethers that link them with the other cells and the proteinaceous matrix in that tissue (Van Noorden, 1998)." The cells are not designed to travel throughout the body and invade other organs. However, the altered metastactic cancers cells are able to sever the links and attack the proteinaceous...

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Instead, they are often "more dangerous than the original, or primary, tumor (Van Noorden, 1998)." These cells starve and dislodge the organ's normal cells, which can be deadly since the organ is unable to function normally with the cancerous cells embedded within it.
ATX

There are protein factors that regulate tumor cell motility. The "secreted factors in the conditioned media of some human melanoma cells is termed autocrine motility hypothesis, which suggests that tumor cells may initiate, sustain, and regulate their own locomotion (home.ccr.cancer.gov/LOP/Research/tumorinv/default.asp)." One factor which is purified from a melanoma cell line is autotaxin (ATX). ATX is a "novel 125 kDa glycoprotein and ectoenzyme that is a potent stimulator or tumor cell motility, invasion, and metastasis. ATX stimulates random and directed motility (ED50~300-500 pM) in a variety of tumor cell lines, including those from prostate and breast carcinomas, melanomas, and neuroblastomas (home.ccr.cancer.gov/LOP/Research/tumorinv/default.asp)." The ATX protein is secreted and synthesized by these cell lines and teratocarcinoma cells.

Homology between family of "cell surface type 1 phosphodiesterases called NPPs (nucleotide phosphodiesterase and pyrophospatases) and ATX was discovered via a cDNA sequence analysis (home.ccr.cancer.gov/LOP/Research/tumorinv/default.asp)." Components of NPPs include a "marker of B cell activiation (PC-1/NPP-1), a neural differentiation antigen (B-10/NPP-3), and ATX (NPP-2). Native ATX possesses phosphodiesterase activity at neutral and alkaline pH, binds ATP non-covalently, and has pyrophosphatase, ATPase, ADPase, and AMPase activities. Homogeneously purified recombinant ATX, based on the teratocarcinoma sequence, retains all of these activities, as well as a capacity to stimulate motility (home.ccr.cancer.gov/LOP/Research/tumorinv/default.asp)." ATX is considered be a factor in metastatic surges through a number of mechanisms, and supports an "invasive…

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